Research

Our lab will explore the molecular mechanisms that allow infectious bacteria to subvert host pathways and promote their own survival. Host cells respond to microbial invasion by encapsulating the pathogen within a membranous compartment that then fuses with a digestive organelle to destroy the enclosed enemy. But some bacteria—including the one that causes Legionnaires’ disease—avoid this fate by directing the fusion of a different set of host membranes, generating for themselves a safe place to reproduce. As a postdoctoral fellow, I discovered that the bacterium Legionella chemically modifies host proteins involved in membrane tethering and fusion. Now, using a suite of cutting-edge techniques in biochemistry, microbiology, cell biology, and molecular genetics, we will determine how this chemical modification allows the bacteria to manipulate and misdirect membrane trafficking in host cells—and identify other host proteins that might be involved in this process. This work could produce novel strategies for combating infections, as well as new tools for investigating fundamental cellular processes.

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